While rejuvenation research aims at a world in which no-one ever suffers coronary artery disease or a heart attack, the causes of those conditions prevented and controlled, we still live in a world in which these conditions are accepted as inevitable, and the near term focus of regenerative medicine is structural repair for the survivors after the fact. This is a poor second best, but the research community continues to develop ever better potential means of repair. In this case, in which researchers provoke greater construction of secondary arteries that can support the primary blood vessels of the heart, capable of supplying blood when the primary is damaged, one may ask whether it can also be a means of reducing the impact of structural damage if applied well in advance. Sadly, preventative medicine of this sort is a hard sell in the present regulatory environment. Applying enhancement therapies to older people still considered "healthy" is just not as acceptable a goal as it should be.
Researchers observed that patients with blockages in major arteries feeding the heart often have confoundingly different outcomes. "Some patients have a blockage in one coronary artery and die; other patients have multiple blockages in multiple areas but can run marathons." The difference may be that this second group of patients has collateral arteries, tiny arteries that bypass blockages in hearts' major arteries and feed areas of the heart starved of oxygen. "They are like the side streets that let you get around a traffic jam on the freeway." Such collateral arteries could help people with atherosclerosis or people recovering from a heart attack, except that collateral arteries are only seen in a minority of patients.
Researchers have now discovered how these collateral arteries are formed and a signaling molecule that promotes their growth in adult mice, offering hope that collateral arteries may be coaxed to grow in human patients. The researchers began by looking at newborn mice. They documented that young mouse healing was due in part to the growth of new collateral arteries into the injured area. Through advanced imaging that let them look at the intact newborn hearts at the cellular level, the researchers showed that this happened because arterial endothelial cells exited the artery, migrated along existing capillaries that extended into injured heart tissue and reassembled to form collateral arteries.
The molecule CXCL12 is an important signal during embryonic development of arterial cells, and has been shown to improve cardiac recovery and function after heart attacks. The scientists wondered if this molecule had a beneficial effect by promoting collateral artery growth in injured heart tissue. They found that CXCL12 was mostly restricted to arterial endothelial cells in uninjured neonatal mouse hearts. In newborn mice with heart injuries, it shows up in the capillaries of the injured area. The researchers found evidence that low oxygen levels in the injured area turned on genes that create CXCL12, signaling the areas to which arterial endothelial cells should migrate.
Next they investigated whether CXCL12 could help adult heart tissue grow collateral arteries. After inducing heart attacks in adult mice, they injected CXCL12 into the injured areas. Sure enough, 15 days after the injuries, there were numerous new collateral arteries formed by the detaching and migrating artery cells. Almost none were present in control mice.